The review states that "sex hormones, androgens and estrogens" are usually involved in the divergent developmental processes that lead to sexual dimorphism, after initially similar precursor structures in both sexes.[2022] It further concludes that "androgen signaling has been identified as the primary factor that establishes male characteristics," with testosterone (T) as "the primary circulating androgen" and dihydrotestosterone (DHT) as its derivative that bind the androgen receptor to drive male-typical development. The paper emphasizes that muscle development and other male-biased traits are "known to be responsive to the effect of testosterone," highlighting a central role for androgen signaling in morphological sexual dimorphism, at least for male traits in mammals.

This minireview states: "Androgen signaling has been identified as the primary factor that establishes male characteristics." It notes that the ligands for androgen signaling are testosterone (T) and dihydrotestosterone (DHT), with T described as "the primary circulating androgen" secreted by Leydig cells. The review emphasizes that the developmental program of external genital formation "has been explained through the dominant effect of androgen signaling" and that masculinization of the male genital tubercle is attributed to active androgen signaling.

This study notes that a "growing body of evidence indicates testosterone can regulate growth, thus the development of [sexual size dimorphism] SSD, and sexual dichromatism." It reports that in phrynosomatid lizards, "sexual divergence in growth is associated with maturational increases in male testosterone levels" in both male- and female-larger species, and that testosterone can either stimulate or inhibit growth depending on the species. The authors conclude that their results suggest "the inhibitory effect of testosterone on growth is mediated by androgen receptors" and that androgens are key endocrine regulators of sex-specific growth patterns, but they also emphasize that sex steroids more broadly (including estrogens) act through the somatotropic axis to generate sex differences in size.

In general, the establishment of phenotypic dimorphisms in rodents (and presumably humans) is generated by different levels of hormones at specific times in XX and XY individuals. Males have an early surge of testosterone, and females a later surge of estrogens. Paradoxically, the testosterone surge in males has the same effect as an estrogen surge, because neurons contain an enzyme (aromatase) that converts testosterone to estradiol. Thus, the surge of testosterone in developing males is, ultimately, converted into a surge of estradiol. In sum, the way that estrogens—the ultimate agents of both female and male sexual differentiation—stimulate sexually dimorphic patterns of development is by binding to estrogen receptors.

The abstract states: "In males it is frequently testosterone (T) that activates the expression of sexually selected morphological and behavioral displays, but the role of T in regulating similar traits in females is less clear." The authors examine red-backed fairy-wrens and conclude that females "have the capacity to express most male-typical traits in response to exogenous T" but that low androgen levels during molt prevent females from developing male-like ornamentation. They summarize that females retain molecular mechanisms for hormonally regulated male-typical ornamentation that are rarely activated because of insufficient hormonal signal.

In the introduction, the paper notes: "Sex-limited secretion of hormones is one such mechanism, either transiently activating or permanently organizing sexually dimorphic character expression in many vertebrates." It further states: "In males it is frequently testosterone (T) that activates the expression of sexually selected morphological and behavioral displays." The study uses GnRH and testosterone manipulations to demonstrate that exogenous testosterone can activate male-typical ornamental traits in females, linking androgen secretion to sexually selected morphological dimorphism.

This review on vertebrate secondary sexual characteristics notes that these traits, which are classic targets of sexual selection, are often regulated by hormones, especially sex steroids. It discusses how androgens such as testosterone frequently mediate the expression of male secondary sexual traits (e.g., ornamentation, weaponry, and behavior), but it also emphasizes that multiple physiological mechanisms, including estrogens and other endocrine pathways, can underlie sexually selected dimorphisms. The paper therefore ties sexual selection to morphological dimorphism via endocrine mechanisms, with testosterone playing a major role for many male traits, while not being the sole hormonal pathway involved.

Testosterone is a key hormone for the development of secondary sexual characters and dimorphisms in behavior and morphology of male vertebrates. Previous comparative analyses in birds and fish demonstrated a relationship between male-to-female testosterone ratios and the degree of sexual dimorphism. The ratio of mean maximum testosterone concentrations of male and female birds was significantly related to the combined dimorphism index or to plumage dimorphism: when dimorphism was low, the ratio of male-to-female testosterone concentrations was lower than when the dimorphism was high. However, the relationship of male-to-female testosterone may not be a good predictor of sex differences in intra- and intersexual competition, and females are likely to use other means to regulate aggression or sexually dimorphic traits such as a colorful plumage.

The authors state that "testosterone is a key hormone for the development of secondary sexual characters and dimorphisms in behavior and morphology of male vertebrates." They analyze male-to-female testosterone ratios across bird species and relate these to the degree of sexual dimorphism and life-history strategies, finding that interspecific variation in testosterone profiles is associated with variation in sexually dimorphic traits. The article frames testosterone as a central endocrine component of an "integrated phenotype" that links sexual selection, male behavior, and morphological dimorphism, while acknowledging that other hormones and ecological factors also contribute.

The review states that dimorphic features of the musculoskeletal system "have been mainly attributed to the action of sex steroid hormones," which influence bone mass, architecture and musculature. It notes that these dimorphic characteristics are "ascribed to high levels of testosterone and insulin-like growth factor-1, resulting in increased muscle mass and strength in boys, whereas estrogens tend to decrease muscle area in girls." The authors also highlight that sex chromosomes contribute, finding that while "gonadal sex is the main contributor" to differences in bone and skeletal muscle mass, sex chromosome complement impacts fat mass.

Cox et al. describe sex steroids as "excellent candidates for the regulation of sex differences in growth and body size because they are produced and secreted in sex-specific fashion by the gonads." Using lizard models, they show that in Anolis sagrei, "castration inhibits, and testosterone stimulates, male growth," and they review other squamate studies indicating that testosterone may act as a "bipotential" regulator by stimulating growth in male-larger species but inhibiting growth in female-larger species. They conclude that "the evolution of [sexual size dimorphism] SSD has been accompanied by underlying changes in the effect of testosterone on male growth," implicating testosterone as an important but evolutionarily flexible endocrine mechanism linking selection on size to dimorphism.

When selection on males and females differs, the sexes may diverge in phenotype. Hormones serve as a proximate regulator of sex differences by mediating sex-biased trait expression. In male birds, plasma testosterone varies seasonally and among species according to mating system. We report that female testosterone also varies seasonally and covaries with male testosterone. Female testosterone is higher in relation to male testosterone in sexually monomorphic species and is higher absolutely in females of species with socially monogamous mating systems, which suggests adaptation. Traits with opposing fitness consequences in males and females could constrain dimorphism, and results from birds reveal many testosterone-sensitive traits, some of which appear costly and may help to account for observed levels of sexual dimorphism.

Cox et al. describe sex steroids as candidates for regulating sex differences in growth: "Sex steroids (i.e. androgens, estrogens and progestins) are excellent candidates for the regulation of sex differences in growth and body size because they are produced and secreted in sex-specific fashion by the gonads." In brown anole lizards, they show that castration inhibits and testosterone stimulates male growth, concluding that "the evolution of SSD [sexual size dimorphism] has been accompanied by underlying changes in the effect of testosterone on male growth, potentially facilitating the rapid evolution of SSD." They also note that in some Sceloporus lizards, testosterone can stimulate growth in male-biased SSD species but inhibit growth in female-biased SSD species, implying complex endocrine control.

This article explains that in many vertebrates, including mammals, "sexual differentiation of the brain" is largely organized by gonadal steroids, particularly androgens that are locally converted to estrogens. In rodents, for example, testosterone secreted by the fetal testes is aromatized to estradiol in the brain, and this estrogenic signaling masculinizes neural circuits and behavior. The paper therefore highlights that even where testosterone is the initial gonadal product, estrogen (via aromatization) can be the proximate endocrine mechanism masculinizing sexually dimorphic brain structures and behaviors, indicating that testosterone is not always the direct effector hormone.

The article opens: "It is widely assumed that the development of male secondary sexual traits in birds and mammals is testosterone-dependent." It then argues that in birds, sexual dimorphism involves at least two mechanisms: male-specific behaviors and structures such as spurs and wattles are typically testosterone-dependent, whereas "bright male plumage is generally believed to be the default developmental state," with ovarian hormones suppressing this state in females. The authors describe how castration of male peafowl does not remove ornate plumage, but removal of ovaries in females induces male-like plumage, challenging a simple view of testosterone as the sole endocrine mechanism.

We have shown that, during male adolescence, testosterone acting through androgen receptor increases the volume of white matter. Age and sex differences in white matter volumes were partially explained by circulating testosterone levels and CAG repeat length in the androgen receptor gene. These findings suggest that testosterone, via the androgen receptor, contributes to sexual dimorphism in the human adolescent brain by influencing both global and regional brain volumes.

The meta-analysis states: "Humans are sexually dimorphic: men and women differ in body build and composition, craniofacial structure, and voice pitch, **likely mediated in part by developmental testosterone.**" It reports that traits such as voice pitch, height, and testosterone predicted mating, while strength/muscularity was the strongest and only consistent predictor of both mating and reproduction. The authors conclude that these results "support arguments that strength/muscularity can be considered sexually selected in humans," implying a link between androgen-mediated traits and sexual selection, though they note that evidence is weaker for other masculine traits.

This review notes that in many vertebrates, sex differences in behavior and morphology are mediated by organizational and activational effects of gonadal steroid hormones, particularly androgens and estrogens. It explains that sex-limited secretion of these hormones can organize and activate sex differences in brain and behavior, and discusses how in some bird species, male-typical traits such as song and certain ornaments are associated with testosterone, while other dimorphic traits are controlled by different hormonal or genetic mechanisms. The authors emphasize that multiple endocrine systems, not only testosterone, contribute to sexual dimorphism.

McCarthy and colleagues review mechanisms of sexual differentiation of the brain and state that gonadal hormones, especially testosterone and its metabolites, are critical for masculinizing neural structures and behavior. They discuss how perinatal testosterone secretion in males, followed by aromatization to estradiol in the brain, produces permanent sex differences in regions such as the preoptic area. However, they also stress that sex differences arise from interacting influences of sex chromosomes, multiple hormones, and environmental factors, indicating that testosterone is a key but not exclusive endocrine mechanism underlying sexually dimorphic traits.

Sex hormones are involved in the sexual dimorphism of the immune response in malaria; oestrogens induce immunocompetence, in contrast, testosterone, the primary male hormone, generates immunosuppression. Testosterone is primarily synthesised in the gonads and increases susceptibility to various bacterial, viral, and parasitic diseases, including malaria. Our results show that testosterone changes affect females more than males, resulting in sex-associated patterns. Testosterone administration increased parasitaemia in intact males while reducing it in intact females, leading to a dimorphic pattern. The results of this work contribute to understanding the impact of modifying testosterone concentration on the immune response specific against Plasmodium and the participation of this hormone in sexual dimorphism in malaria.

This review explains that sex differences in body growth, composition and adipose tissue distribution are largely governed by sex steroids. It highlights that androgens, particularly testosterone, promote linear growth and lean body mass in males while inhibiting fat accumulation in certain depots, whereas estrogens have distinct effects on female growth and fat patterning. The authors describe sex steroids as major endocrine regulators of sexually dimorphic somatic traits but also mention contributions from growth hormone, IGF-1 and other endocrine factors, emphasizing a multifactorial hormonal basis.

We tested whether testosterone dimorphism was associated with paternal care and sexual size dimorphism while accounting for sampling matrix and phylogeny. Across vertebrates, sexual dimorphism in testosterone levels was positively associated with the degree of male-biased sexual size dimorphism. Species in which males had much higher testosterone than females tended to exhibit stronger male-biased size dimorphism. However, the authors emphasize that testosterone dimorphism explained only part of the variation in sexual size dimorphism, indicating that other endocrine and developmental mechanisms also contribute.

This classic review links sexual dimorphism to sexual selection and discusses the role of sex hormones in mediating dimorphic traits. It notes that in many mammals, testosterone promotes male-typical characteristics such as larger body size, weaponry and aggressive behavior that are targets of sexual selection. At the same time, it points out that dimorphism can also be influenced by ecological factors, developmental constraints and other hormonal systems, cautioning against attributing sexual dimorphism to a single endocrine mechanism even when testosterone plays a central role in many cases.

This review discusses how sexual selection shapes sexually dimorphic traits via hormonal mechanisms. In many vertebrates, testosterone and other androgens mediate the development and expression of male-typical ornaments, weapons, and behaviors that are favored by sexual selection. However, the authors stress that testosterone is only one component of a broader endocrine system. Estrogens, glucocorticoids, and peptide hormones, along with variation in receptor densities and local metabolism of steroids, also influence the degree and direction of sexual dimorphism. Thus, sexual selection translates into morphological and behavioral differences between the sexes through multiple hormonal pathways rather than a single principal endocrine mechanism.

This university teaching page explains that in mammals, "sexual dimorphism in which males are larger in size or have more prominent weapons is often associated with **polygynous mating systems**," indicating a role of sexual selection in shaping male-biased traits. It notes that male traits like antlers and large body size develop under the influence of **androgens** and confer advantages in male–male competition and mate attraction, connecting endocrine mechanisms with sexually selected morphological dimorphism.

The article defines sexual dimorphism as differences in morphology between sexes, often arising through sexual selection. It notes that in humans, "Pubertal changes in males lead to a tenfold increase in testosterone compared to females" and that "It is because of the effects of testosterone that males develop stronger and denser bones, as well as increased muscle mass and strength during puberty." It also explains that sexual differentiation in the human brain is triggered by fetal testicular testosterone, which is aromatized to estrogen in the brain, demonstrating an endocrine pathway from androgens to sexually dimorphic morphology and neural traits.

The overview states that sexual dimorphism involves "physical differences between a species' male and female members" and notes that such differences "may include variation in size, color, or the presence of elaborate structures." It explains that sexual dimorphism "often results from **sexual selection**, in which traits that improve mating success become more pronounced," and that hormones such as **testosterone** play a key role in the development and maintenance of many male secondary sexual characteristics.

This comparative review examines how both testosterone and estradiol relate to sexually selected traits in birds. It reports that interspecific variation in male testosterone levels correlates with the expression of some male ornaments and aggressive behaviors, but also finds cases where estradiol and other hormones better explain certain aspects of sexual dimorphism. The authors argue that sexual selection operates on an integrated endocrine system in which testosterone is often prominent but interacts with estrogens, corticosterone, and other hormonal pathways to generate dimorphic traits.

This integrative review summarizes that sexual dimorphism in vertebrates arises from interactions among sex chromosomes, gonadal differentiation, and endocrine signaling. It emphasizes that while androgens, particularly testosterone, are central to the development of many male-typical traits, estrogens, growth hormone, and other endocrine factors also contribute to dimorphic morphology and physiology. The authors argue that selection on sexually dimorphic traits can act on any component of this endocrine network, suggesting there is no single "principal" hormonal route by which sexual selection is translated into morphological dimorphism across vertebrates.

Across vertebrates, testosterone is widely documented as a major androgen linking sexual selection to sexually dimorphic traits, especially male-biased ornaments, weapons, musculature and behaviors. However, research also identifies important roles for other androgens (like DHT), estrogens, progesterone, pituitary hormones (e.g., LH, FSH), and direct genetic sex-chromosome effects in producing dimorphism. Empirical work in birds, reptiles and mammals shows that some dimorphic traits arise from suppression in females or sex-specific gene regulation rather than exclusively from testosterone-driven enhancement in males, indicating no single universal endocrine mechanism.